[Controlled clinical studies on statins have produced evidence that the aggressive lowering of LDL-cholesterol (LDL-C) level reduces the mortality rate of ischaemic heart disease. About 40% of treated patients achieve the cholesterol target level. The observance of medication instructions on a daily basis (compliance) and willingness for long-term taking of the drug (persistence) are crucially important to avoid severe complications. In the long term, patients take only about 50% of their medicines according to the instructions. As a result of the generally poor compliance and persistence in taking the medications, the decrease in morbidity and mortality observed in clinical studies do not occur under real-life conditions. Patients with poor compliance (<80%) will experience only a minimal health benefit and the cost-effectiveness of the therapy will markedly decrease. For patients with poor persistence who discontinue their treatment before benefits at the clinical endpoints could manifest, the resources invested into the therapy will be lost. Both compliance and persistence deteriorate as the number of concurrently taken medicines increases. Since less than 50% of the programmes aimed at improving patient co-operation are successful, therapeutic decisions should preferably be made by taking into consideration the expected compliance/persistence already at the time of choosing the medication. By widening the use of fixed-dose combination therapies, the efficiency of treatment can substantially be increased in patients who concurrently take several medicines and require aggressive lowering of blood pressure or LDL-C level.]

[Disturbances in ventricular relaxation may lead to the development of diastolic heart failure. The analysis of left ventricular endomyocardial biopsy specimens may help understand the underlying structural and functional changes. Such analyses have lead to the recognition that at the optimal sarcomere length of the Frank- Starling mechanism (i.e., at 2.2 μm), passive force values of the cardiomyocytes are significantly higher in individuals with diastolic heart failure than in healthy controls. As a probable explanation to this finding, increased expression of the stiffer N2B isoform of the myofilamental titin protein, at the expense of the more elastic N2BA titin isoform, has been recognized. Moreover, decreased phosphorylation of the contractile proteins was also suggested to contribute to the development of diastolic heart failure. These changes together, and along with an increase in extracellular collagen content, may greatly contribute to the relaxation disturbance observed in diastolic heart failure.]